Abstract |
Type 2 diabetes (T2D) is a chronic disease caused by pancreatic β-cell dysfunction and insulin resistance. Exposure to smoke is a risk factor for diabetes; however, its mechanisms are unclear. In an epidemiological study, we determined the relationship between cigarette smoking and β-cell function. T2D patients had a history of heavier smoking than people without T2D, and heavy smokers had more abnormal glucose metabolism. For various smoking populations, there was a dose-effect relationship between decreases of homeostatic model assessment (HOMA)-β levels or the increases of HOMA- insulin resistance (IR) levels and amount of smoking (pack-years), which indicated that smoking induced β-cell dysfunction. For MIN6 cells, cigarette smoke extract (CSE) decreased insulin secretion and content; enhanced apoptosis, as illustrated by decreases of BCL-2 levels, increases of BAX and cleaved caspase-3 levels, and an increased apoptotic index; and activated the p38 MAPK pathway. For MIN6 cells, inhibition of p-p38 MAPK by SB203580 prevented enhanced apoptosis and the dysfunction of insulin secretion induced by CSE. In sum, activation of p38 MAPK is involved in the apoptosis of pancreatic β-cells induced by cigarette smoking, which is a possible mechanism for induction of T2D by cigarette smoke.
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Authors | Hui Xu, Qiushi Wang, Qian Sun, Yu Qin, Aohan Han, Ye Cao, Qianlei Yang, Ping Yang, Jiachun Lu, Qizhan Liu, Quanyong Xiang |
Journal | Environmental science and pollution research international
(Environ Sci Pollut Res Int)
Vol. 25
Issue 10
Pg. 9817-9827
(Apr 2018)
ISSN: 1614-7499 [Electronic] Germany |
PMID | 29372523
(Publication Type: Journal Article)
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Chemical References |
- Smoke
- Cholestyramine Resin
- p38 Mitogen-Activated Protein Kinases
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Topics |
- Adult
- Animals
- Apoptosis
(drug effects)
- Cell Line, Tumor
- Cholestyramine Resin
- Cigarette Smoking
(adverse effects)
- Cross-Sectional Studies
- Diabetes Mellitus, Type 2
(enzymology, etiology, pathology)
- Humans
- Insulin-Secreting Cells
(drug effects, pathology)
- Male
- Mice
- Smoke
(adverse effects)
- p38 Mitogen-Activated Protein Kinases
(metabolism)
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